Fig. 3: A key structural–functional network between the cardiac L-type calcium channel and mitochondria assists in regulating mitochondrial function under conditions of varying substrate stiffness. | Communications Biology

Fig. 3: A key structural–functional network between the cardiac L-type calcium channel and mitochondria assists in regulating mitochondrial function under conditions of varying substrate stiffness.

From: A maladaptive feedback mechanism between the extracellular matrix and cytoskeleton contributes to hypertrophic cardiomyopathy pathophysiology

Fig. 3

Representative ratiometric flavoprotein (a, b and g, h) and JC-1 (d, e and j, k) fluorescence recorded from wt cardiac myocytes plated on soft and stiff hydrogels before and after exposure to 10 μM BayK(+), or 10 μM BayK(−) in the absence or presence of AID-TAT (10 μM), AHNAK-P4N-TAT (1 μM), Latrunculin A (Latrunc, 5 μM, 20 min pre-incubation) or Colchicine (Colch, 1 μM, 3 h pre-incubation51). JC-1 studies were performed under calcium-free conditions (0 mM calcium). Arrows indicate addition of drugs. To confirm signals were mitochondrial in origin, FCCP (50 μM) was applied at the end of each flavoprotein experiment to increase flavoprotein oxidation. NaCN (40 mM) was applied at the end of each JC-1 experiment to collapse Ψm. Overall flavoprotein (c and i) and JC-1 (f and l) fluorescence for all myocytes (n) exposed to drugs as indicated, including mean ± SEM. All statistical significance determined by Kruskal-Wallis tests.

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